A patient on standard anti-TB therapy (HRZE) develops optic neuritis with loss of red-green colour discrimination. The drug responsible and the mechanism of toxicity is:

• A Isoniazid – inhibits pyridoxal phosphate-dependent enzymes in optic nerve axons
• B Rifampicin – induces CYP450 enzymes reducing retinal antioxidant concentrations
• C Pyrazinamide – uric acid accumulation in the optic canal causes compressive neuropathy
• D Ethambutol – accumulates in optic nerve, chelating zinc and inhibiting arabinosyl transferase enzyme ✓

Explanation

Ethambutol-induced optic neuropathy is the classic dose-related ocular toxicity of anti-TB therapy, presenting with reduced visual acuity and impaired red-green colour discrimination (centrocecal scotoma in optic neuritis). The mechanism involves ethambutol chelating zinc ions from retinal ganglion cells and optic nerve axons, disrupting zinc-dependent enzymes in axonal mitochondria. Baseline and monthly visual acuity and colour vision testing is mandatory; the drug should be stopped immediately on any visual symptom.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.